Lactic acid plays a central role in the metabolism of vascular smooth muscle. A large fraction of the ATP produced by vascular smooth muscle is via glycolysis, even under aerobic conditions. Lactate oxidation can also serve to generate ATP for the contraction of vascular smooth muscle. It has usually been assumed that lactate enters and leaves muscle cells by simply diffusing across the plasma membrane. Recent evidence suggests that lactate transport in skeletal muscle occurs by mediated transport and there is good evidence that lactate transport is carrier-mediated in human erythrocytes. Recent work in our laboratory suggests that exogenous lactate enters the cells of rat aortic smooth muscle by a carrier-mediated mechanism. Alterations in the metabolism of vascular smooth muscle are certainly involved in the microangiopathy of human diabetes mellitus. The frequent incidence of atherosclerosis in diabetic patients also points to metabolic abnormalities of vascular smooth muscle in diabetes. Abnormalities in the metabolism of carbohydrates and amino acids by vascular smooth muscle have been documented in experimental diabetes in several species, but lactate metabolism in vascular smooth muscle has not been studied in diabetes. There is evidence that in alloxan diabetic animals lactate metabolism is abnormal in skeletal and cardiac muscle. We propose to continue our studies of lactate transport and metabolism of vascular smooth muscle in normal rat aorta and in aortas from alloxan diabetic rats. Our principal purposes are to (1) better characterize the processes by which lactate enters and leaves vascular smooth muscle cells and (2) investigate abnormalities in lactate metabolism in vascular smooth muscle from diabetic animals.